Fig. 8: Summary of the role of ATM downregulating MHC-I expression by inactivating the c-Jun/TNF-α/p-STAT1 signaling axis in TNBC. | Cell Death & Disease

Fig. 8: Summary of the role of ATM downregulating MHC-I expression by inactivating the c-Jun/TNF-α/p-STAT1 signaling axis in TNBC.

From: Inhibition of ATM enhances the immunogenicity of triple-negative breast cancer by promoting MHC-I expression

Fig. 8

The Schematic model summarizes the promotion effect of ATM/c-Jun/TNF-α/p-STAT1 signaling axis on MHC-I expression in TNBC. ATM inhibition upregulates TNF-α expression at both transcriptional and translational levels by promoting c-Jun phosphorylation and nuclear translocation, thereby enhancing its binding to the TNF-α promoter region. The elevated TNF-α subsequently facilitates STAT1 phosphorylation through TNFR1-STAT1 interaction, ultimately mediating increased expression of both MHC class I and PD-L1 molecules. The up-regulation of PD-L1 molecules is the result of the regulation of ATM/JNK/c-Jun/TNF-α signaling axis confirmed by our previous study [33].

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